Mobil Oil Corp. v. Bailey

187 S.W.3d 265, 2006 WL 560584

• Court: Court of Appeals of Texas
• Decided: April 13, 2006
• Docket: 09-04-225-CV
• Status: Published

Opinions

OPINION

CHARLES KREGER, Justice.

Pearlie Bailey, individually and as ad-ministratrix of the Estate of James E. Bailey, deceased, James Thibodeaux, Kevin Bailey, Paul Bailey, and Carolyn Bailey (“Baileys”) sued Mobil Oil Corporation, Mobil Oil Refining Corporation, and Mobil Chemical Company, Inc. (“Mobil”) for the wrongful death of James Bailey from lung cancer. The Baileys’ suit alleged James’s death was caused by his exposure to asbestos on Mobil’s premises. The jury found Mobil’s negligence caused James’s death and awarded $350,000 in actual damages (most of the actual damages were offset by settlement credits). Further, the jury found the harm to James resulted from malice and awarded $500,000 in exemplary damages. The trial court denied Mobil’s post-trial motions and entered judgment on the verdict. From that judgment, Mobil brings this appeal. Because we find the Baileys presented no evidence of probative force of medical causation, we sustain issue two, reverse the trial court’s judgment, and render judgment in favor of Mobil.

BACKGROUND

It is not disputed that James worked at Mobil’s Beaumont, Texas, facilities sporadically from the years 1966 to 1972. James’s work assignments on Mobil’s premises subjected him to asbestos exposure in varying degrees of severity. His work history also indicated he had been exposed to asbestos at other work sites, including ships, furnaces, and as an operator helper. The record also indicates that James was a long-time smoker, and that for the last forty to fifty years of his life, he smoked a full pack of cigarettes per day. Neither party disputes the fact that there was a total absence of medical evidence typifying asbestos exposure, such as the presence of asbestos bodies in James’s lungs, scarring of his lung tissue, or pleural thickening.

As noted above, the Baileys’ theory of the cause of James’s lung cancer was severe asbestos exposure while working at Mobil’s facilities. By contrast, Mobil’s theory was that James’s heavy smoking history alone caused his lung cancer because of the complete absence of asbestos-related indicators in his lungs. As such, medical causation was the key issue at trial and is at the heart of Mobil’s appeal. Mobil raises nine appellate issues, with issue one contending trial error “in admitting the testimony of Plaintiffs’ experts on medical causation,” and issue two raising the lack of “legally sufficient evidence to support the jury’s finding that Mr. Bailey’s lung cancer was proximately caused by Mobil’s conduct in exposing him to asbestos at Mobil’s facilities.”

STANDARD OF REVIEW

In E.I. du Pont de Nemours and Co. v. Robinson, 923 S.W.2d 549, 550 (Tex.1995), a products liability case, the Texas Supreme Court determined the proper standard for the admission of scientific expert testimony under Rule 702 of the Texas Rules of Civil Evidence.¹ Relying on language contained in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579, 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993), the Robinson Court held that “in addition to showing that an expert witness is qualified, Rule 702[²] also requires the proponent to show that the expert’s testimony is relevant to the issues in the case and is based upon a rehable foundation.” Robinson, 923 S.W.2d at 556. The Robinson Court relied on Daubert for support, viz:

Rule 702 requires the proffered testimony to be: (1) “scientific knowledge” (2) which will “assist the trier of fact to understand the evidence or to determine a fact in issue.” Id. at 589, 113 S.Ct. at 2795 (quoting FED. R. EVID. 702). To constitute “scientific knowledge,” the proffered testimony must be reliable. Id. In addition, to be helpful to the trier of fact, the evidence must be relevant. Scientific evidence is relevant when there is a “valid scientific connection to the pertinent inquiry as a precondition to admissibility.” Id. at 592, 113 S.Ct. at 2796.

Robinson, 923 S.W.2d at 555.

There is no question that Robinson’s relevant/reliable requirements were preconditions for admissibility only. Indeed, the Court noted that “legal sufficiency of scientific evidence” was an inquiry “outside the scope of Rule 702.” Id. at 554. At present, Robinson continues to be the seminal case with regard to admissibility of any type of expert testimony, including scientific testimony, in Texas.

In 1997, the Texas Supreme Court handed down Merrell Dow Pharmaceuticals, Inc. v. Havner, 953 S.W.2d 706 (Tex.1997). The Court framed the issues in Havner, another products liability case, in the following manner:

Merrell Dow challenges the legal sufficiency of the Havners’ causation evidence and the admissibility of some of that evidence and further contends that its due process rights under the United States Constitution and its due course rights under the Texas Constitution were denied. Because of our disposition of this case, we reach only the no evidence point of error.

Id. at 709. Although it limited review to the legal sufficiency inquiry only, the Hav-ner Court proceeded to incorporate the admissibility standards announced in Robinson into the standard for reviewing no evidence appellate issues. See id. at 711, 712, 714 (“The issue in Robinson was admissibility of evidence, but as we have explained the same factors may be applied in a no evidence review of scientific evidence.”).³

The Havner Court’s development of its no evidence analysis in toxic tort cases takes a stricter approach than that applied in a traditional no evidence review, as is evidenced by the following:

It could be argued that looking beyond the testimony to determine the reliability of scientific evidence is incompatible with our no evidence standard of review. If a reviewing court is to consider the evidence in the light most favorable to the verdict, the argument runs, a court should not look beyond the expert’s testimony to determine if it is reliable. But such an argument is too simplistic. It reduces the no evidence standard of review to a meaningless exercise of looking to see only what words appear in the transcript of the testimony, not whether there is in fact some evidence. We have rejected such an approach. See Schaefer [v. Texas Employers’ Ins. Ass’n], 612 S.W.2d [199,] 205 [(Tex.1980)]; see also Burroughs Wellcome [Co. v. Crye], 907 S.W.2d [497,] 499-500 [(Tex.1995)].

[[Image here]]

Although we recognize that there is not a precise fit between science and legal burdens of proof, we are persuaded that properly designed and executed epidemiological studies may be part of the evidence supporting causation in a toxic tort case and that, there is a rational basis for relating the requirement that there be more than a “doubling of the risk” to our no evidence standard of review and to the more likely than not burden of proof.

Havner, 953 S.W.2d at 712, 717 (some citations omitted).

At any rate, the Havner Court’s no evidence standard applied to toxic-tort litigants attempting to demonstrate that exposure to a given substance increased the risk of the particular injury alleged when direct, scientifically rehable proof of causation was missing. Id. at 715. Such litigants are reduced to relying entirely on circumstantial evidence in the form of scientific studies for proof of causation. Id. In their attempt to link the limb reduction birth defect with the drug Bendectin, the Havner plaintiffs relied on epidemiological studies examining existing populations. Id. at 724-25. To raise a fact issue on causation, the Havner’s epidemiological studies were required to establish a “more than doubling of the risk” that this birth defect, when compared to the same birth defect in an unexposed or “control” population, was attributable to the mother’s Bendectin ingestion during pregnancy. Id. at 715-17, 724-26. In addition to requiring that the scientific evidence establish “more than a doubling of the risk,” the Havner Court’s no evidence standard also encompassed the following:

To raise a fact issue on causation and thus to survive legal sufficiency review, a claimant must do more than simply introduce into evidence epidemiological studies that show a substantially elevated risk. A claimant must show that he or she is similar to those in the studies. This would include proof that the injured person was exposed to the same substance, that the exposure or dose levels were comparable to or greater than those in the studies, that the exposure occurred before the onset of injury, and that the timing of the onset of injury was consistent with that experienced by those in the study. ... Further, if there are other plausible causes of the injury or condition that could be negated, the plaintiff must offer evidence excluding those causes with reasonable certainty. See generally E.I. du Pont de Nemours & Co. v. Robinson, 923 S.W.2d 549, 559 (Tex.1995) (finding that the failure of the expert to rule out other causes of the damage rendered his opinion little more than speculation); Parker v. Employers Mwt. Liab. Ins. Co., 440 S.W.2d 43, 47 (Tex.1969) (holding that a cause becomes “probable” only when “in the absence of other reasonable causal explanations it becomes more likely than not that the injury was a result.”)

Hamer, 953 S.W.2d at 720.

The Supreme Court once again revisited the “no evidence” standard of appellate review in the recent ease of City of Keller v. Wilson, 168 S.W.3d 802 (Tex.2005). In City of Keller, the Court answered the question — “Must an appellate court reviewing a verdict for legal sufficiency start by considering all the evidence” or by considering only evidence favorable to the verdict and disregarding any evidence to the contrary. The Court concluded the two standards are, in effect, the same: “properly applied[,]” they “arrive at the same result[.]” Id. at 827. As the Court explained, “Whether a reviewing court begins by considering all the evidence or only the evidence supporting the verdict, legal-sufficiency review in the proper light must credit favorable evidence if reasonable jurors could, and disregard contrary evidence unless reasonable jurors could not.” Id. at 827. “Contrary evidence” may not be disregarded “if there is no favorable evidence” or if contrary evidence “renders supporting evidence incompetent” or “conclusively establishes the opposite.” Id. at 814-18. A jury’s credibility determinations must be examined for reasonableness; this means that jurors may not ignore undisputed testimony that is “clear, positive, direct, otherwise credible, free from contradictions and inconsistencies, and could have been readily controverted.” Id. at 820 (footnote omitted).

When reviewing a “no evidence” challenge to expert testimony, “ ‘[the] expert’s bare opinion’ ” does not constitute “some evidence,” and “ ‘[t]he substance of the testimony must be considered.’ ” See Kerr-McGee Corp. v. Helton, 133 S.W.3d 245, 254 (Tex.2004) (quoting Hamer, 953 S.W.2d at 711). Additionally, the “ ‘underlying data should be independently evaluated in determining if the opinion itself is reliable.’ ” Id. (quoting Hamer, 953 S.W.2d at 713). “The proponent of the evidence bears the burden of demonstrating that the expert’s opinion is reliable.” Id. (citing Robinson, 923 S.W.2d at 557). “If the expert’s testimony is not reliable, it is not evidence.” Id. (citing Hamer, 953 S.W.2d at 713). The Court in Helton then provided a condensed rationale for holding unreliable expert testimony to be “no evidence”:

The reliability requirement focuses on the principles, research, and methodology underlying an expert’s conclusions. Exxon Pipeline Co. v. Zwahr, 88 S.W.3d 623, 629 (Tex.2002). Under this requirement, expert testimony is unreliable if it is not grounded “ ‘in the methods and procedures of science’ and is no more than ‘subjective belief or unsupported speculation.’ ” Id. (quoting Daubert v. Merrell Dow Pharms. Inc., 509 U.S. 579, 590 113 S.Ct. 2786, 125 L.Ed.2d 469 (1993)). Expert testimony is also unreliable if the court concludes that “ ‘there is simply too great an analytical gap between the data and the opinion proffered.’ ” Gammill v. Jack Williams Chevrolet, Inc., 972 S.W.2d 713, 726 (Tex.1998) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146, 118 S.Ct. 512, 139 L.Ed.2d 508 (1997)). In reviewing the reliability of expert testimony, the court is not to determine whether the expert’s conclusions are correct; rather, the court should determine only whether the analysis used to reach those conclusions is reliable. Zwahr, 88 S.W.3d at 629 (citing Gammill, 972 S.W.2d at 728).

Helton, 133 S.W.3d at 254.

Toxic tort cases usually require proof of both “general” and “specific” causation with regard to the effects of the toxic substance. Frias v. Atlantic Richfield Co., 104 S.W.3d 925, 928 (Tex.App.Houston [14th Dist.] 2003, pet. denied)(cit ing Havner, 953 S.W.2d at 714). “General causation exists when a substance is capable of causing a particular injury or condition in the general population, while specific causation exists when a substance causes a particular individual’s injury.” Daniels v. Lyondell-Citgo Refining Co., 99 S.W.3d 722, 725-26 (Tex.App.-Houston [1st Dist.] 2003, no pet.)(eiting Havner, 953 S.W.2d at 714). Proving one type of causation does not necessarily prove the other, and both are needed in situations where direct, reliable medical testing for specific causation has not taken place. See generally Havner, 953 S.W.2d at 714-15.

APPLICATION OF LAW TO FACTS

We must first address the Baileys’ contention that Mobil has waived its issue complaining of the trial court’s failure to exclude plaintiffs’ causation experts for failure to meet the Havner/Robinson reliability standards. The record indicates that prior to the beginning of testimony, Mobil filed written objections to the Baileys’ causation testimony grounded in the standards discussed in Havner, Robinson, and Daubert. In Coastal Transport Company, Inc. v. Crown Central Petroleum Corporation, 136 S.W.3d 227, 232-33 (Tex. 2004), the Supreme Court clarified its holding in Maritime Overseas Corporation v. Ellis, 971 S.W.2d 402, 409 (Tex.1998), where the court stated that “[t]o preserve a complaint that scientific evidence is unreliable and, thus, no evidence, a party must object to the evidence before trial or when the evidence is offered.” Coastal Transport Co., 136 S.W.3d at 232-33 (quoting Maritime Overseas Corp., 971 S.W.2d at 409). Mobil’s written Havner/Robinson objections filed prior to the start of testimony clearly were timely and preserved the issue for appellate review.

At the time of trial, Bailey was one of three plaintiffs alleged to have contracted asbestos-related illnesses, from asbestos exposure. The other two plaintiffs, Ruth Ladner and Joyce Myers, are not parties to the instant appeal. The record indicates that although Bailey, Ladner, and Myers claimed asbestos exposure was the cause of their medical infirmity, the circumstances of exposure were unique to each individual as were their personal habits and the resulting physical manifestations. One plaintiff, Ladner, was diagnosed with asbestosis. She had a minimal smoking history and her exposure purportedly' came from washing her husband’s asbestos-exposed work clothes “several times a week” for about twenty-seven years. Ladner’s husband worked in the petro-chemical industry for a number of years. The second plaintiff, Myers, alleged that she contracted mesothelioma from washing the asbestos-exposed work clothes of her father, an insulator at Mobil, on a more intermittent basis during the times she lived with him which totaled approximately sixteen years. Myers also had a minimal smoking history. However the Baileys’ expert, Dr. Gary Friedman, testified that there is no relationship at all between smoking and mesothelioma because the disease does not start in the lungs, but outside the lungs.

Because of Ladner’s and Myers’ illnesses, the jury was provided with a great deal of testimony and related medical and scientific evidence relating to asbestos exposure and its role in the diseases asbestosis and mesothelioma. This would explain, in part, why much time and effort were spent by plaintiffs offering proof of general causation — that asbestos is a known carcinogen, and exposure to asbestos raises the risk that the exposed person could eventually develop a variety of asbestos-related diseases, such as asbestosis, mesothelioma, and lung cancer.

As the proponent of expert testimony, the Baileys had the burden to raise a fact issue as to specific causation, i.e., to offer competent evidence that asbestos exposure, more likely than not, caused James’s lung cancer, and also to negate with reasonable certainty James’s heavy smoking history as the other plausible cause of his lung cancer. See Havner, 953 S.W.2d at 720. The Baileys’ medical causation experts were Dr. Gary Friedman and Dr. Richard Lemen. On appeal, the Baileys contend these witnesses provided scientifically reliable evidence to prove James’s exposure to asbestos at Mobil’s facilities more likely than not was the cause of his lung cancer. It is true that the record includes Dr. Friedman’s testimony that James’s “combined exposures” to asbestos at Mobil’s facilities doubled his risk for lung cancer. It is also true that Dr. Le-men testified to a “synergistic effect” when a smoker is exposed to asbestos in that the smoker’s risk for eventually developing lung cancer “jumps well over 50 percent.” In support of their causation experts’ testimony, the Baileys direct our attention to certain “scientific literature” upon which Drs. Friedman and Lemen relied for their respective opinions. Some of this scientific literature we have been able to locate as exhibits in the record and some we have not.

In none of the exhibits to which the Baileys have directed us is the employed methodology entirely clear, given that the authors of the studies admit to knowledge of studies reaching the opposite results. For example, in Plaintiffs’ Exhibit 16, “Asbestos and the Histogenesis of Lung Carcinoma”⁴ the authors note that “experimental data confirm the synergism between cigarette smoke and asbestos[.]” However, the authors provide this caveat early in the article:

WHO HAS STUDIED THE RELATIONSHIP BETWEEN ASBESTOS AND BRONCHOGENIC CARCINOMA?

Epidemiologists, occupational physicians, radiologists, pathologists, and biologists have addressed the problem. Each discipline looks at the problem from a different perspective, has its own methodology and its own literature, and answers the questions in different terms. General conclusions are best made only when the limitations of each discipline are appreciated and when the results of the different disciplines are synthesized.⁵

The authors continue by suggesting the theory that asbestos causes lung cancer in the absence of asbestosis is not settled.

MUST PULMONARY FIBROSIS OR ASBESTOSIS BE PRESENT IN THE LUNG TO ATTRIBUTE THE CARCINOMA TO ASBESTOS?

Although the requirement of coexistent carcinoma and asbestosis to make etiologic attribution is convenient, basic biologic principles suggest that this approach is oversimplified and not correct. Inability to integrate experimental results with pathological and then epidemiological studies contributed to delay in accepting the fact that asbestos could cause carcinoma and now hinders appreciation that asbestos can cause carcinoma in the absence of asbestosis. (footnotes omitted)(emphasis added).⁶

The concluding paragraph to this article raises significant concerns as to both the relevance and the reliability for use by either of the Baileys’ causation experts, viz:

TO WHAT DEGREE CAN WE BE CERTAIN THAT ASBESTOS CAUSED OR CONTRIBUTED TO A BRON-CHOGENIC CARCINOMA?

Based on the issues raised here, there are eight possible conclusions (or variations thereof) on the relationship between asbestos and a bronchogenic carcinoma after examining lung tissue of an individual. These possibilities are listed in Table 4. Some are mutually exclusive. These conclusions do not take into account the exposure history of the patient.⁷

Indeed, conclusion 6 listed in Table 4 of the article, as to the degree of certainty that asbestos caused or contributed to an individual’s lung cancer after examining lung tissue states, “Certain that asbestos did not cause the carcinoma because no asbestos is found[,]” while conclusion 5 states, “Possible, but cannot say because no asbestos is found.”⁸ Neither of the Baileys’ causation experts explained the bases underlying their reliance on the information in Plaintiffs’ Exhibit 16, nor what part or parts of Plaintiffs’ Exhibit 16 had general acceptance in the current scientific community. As the Court in Earner has instructed:

If the foundational data underlying opinion testimony are unreliable, an expert will not be permitted to base an opinion on that data because any opinion drawn from that data is likewise unreliable. Further, an expert’s testimony is unreliable even when the underlying data are sound if the expert draws conclusions from that data based on flawed methodology. A flaw in the expert’s reasoning from the data may render reliance on a study unreasonable and render the inferences drawn therefrom dubious. Under that circumstance, the expert’s scientific testimony is unreliable and, legally, no evidence.

Hamer, 953 S.W.2d at 714.

Plaintiffs’ Exhibit 17, titled “Asbestos Inhalation, Not Asbestosis, Causes Lung Cancer,” is a commentary written by Dr. Jerrold L. Abraham, M.D.⁹ His thesis appears to be that, from a medical perspective, it is entirely immaterial whether an individual must be diagnosed with asbestosis before a subsequent diagnosis of lung cancer can be attributed to asbestos exposure or not. Because asbestosis is itself a disease, not an agent of disease, Abraham argues that it would be more “logical” to say that “asbestos inhalation causes both asbestosis and lung cancer and that the majority of persons who have either of these two diseases related to asbestos exposure have had sufficient exposure to result in lung fibrosis.”¹⁰ The fact that something may be thought to be more “logical” is not sufficient to establish causation. Further observations by Abraham echo ones made by the Court in Havner, and place the controversy in proper context: ¹¹

The final issue that needs more open dialogue is the medico-legal implications of all this discussion of “causation” related to asbestos. There is the potential for at least the appearance of many conflicts of interest in this area. Nearly all who write scientific articles in this field sooner or later get called upon to serve as expert witnesses for either plaintiffs or defendants, or both. All who write or edit in this field must be extremely careful to not give the impression that the article in a medical journal is serving the interests of litigation before the interests of science. Owing to different legal rules for proof (“more likely than not”) versus scientific ones (“greater than 95% probability” or “beyond a reasonable shadow of a doubt”), articles such as Dr. Churg’s editorial, while useful in stimulating scientific discussion and further research, might be kept in perspective if they included a brief discussion of the article’s medico-legal ramifications.

[[Image here]]

There is no question that Churg [1993a] is correct in stating: “Probably the most contentious question in regard to asbestos is the relationship between asbestos exposure and the development of carcinoma of the lung” (p. 64). Perhaps open discussion of all the factors involved in this controversy can expedite its resolution.

Dr. Abraham’s commentary does not purport to be an epidemiological article containing explanations of detailed epidemiological studies; instead, it is a reply to a “recent editorial on asbestos and lung cancer by Dr. Andrew Churg [1993b].”¹² Indeed, it would seem that Dr. Abraham’s commentary raises more questions regarding the scientific methodology in this area than it answers, as noted in the following: ¹³

A second major problem with attempts to link asbestosis and lung cancer is that different studies have radically different thresholds for defining/recognizing asbestosis. Is it to be required that someone has radiologic asbestosis > 1/0 ILO category to have lung cancer attributed to asbestos, or do they need biopsy proven asbestosis? Grade 1 of the NIOSH/CAP criteria [Craighead et ah, 1982] is not even termed asbestosis by Churg now [1993a], (but rather asbestos-airway disease), so even the pathologic criteria would have to be clearly defined ....

While highly informative, we find that Dr. Abraham’s commentary is simply not an epidemiological study with factors such as those described in Robinson, and, therefore, without sufficient indicia of reliability so as to provide objective, independent validation of the causation experts’ methodology in reaching their opinion on the cause of James’s lung cancer. See Robinson, 923 S.W.2d at 557. These Robinson “admissibility” factors may also be applied in a no evidence review of scientific evidence. See Havner, 953 S.W.2d at 714.

Plaintiffs’ Exhibit 18 consists of a study published in the April 29,1995, issue of the British medical journal, The Lancet, and was “designed to test the hypothesis that the risk of lung cancer from asbestos exposure is confined to persons with radio-graphic evidence of pulmonary fibrosis.”¹⁴ From all appearances, it would seem this study was conducted under recognized scientific methodology with the various results subjected to statistical significance. The results of the study “suggest that asbestos is associated with lung cancer even in the absence of radiologieally apparent pulmonary fibrosis.”¹⁵ However, one questionable factor noted in the study and not explained or resolved by either of the Baileys’ causation experts is the authors’ mention of two other epidemiological studies, one involving male “asbestos-cement workers in Louisiana, USA, and the other asbestos miners in South Africa.”¹⁶ The Louisiana study “found no excess of lung cancer in workers without small opacities on the chest radiograph, even among long-term workers,” and it was particularly noted that in workers followed for at least 20 years from first exposure and having no “small opacities” on chest x-rays, “only 10 developed respiratory cancers, whereas 9.5 were expected.”¹⁷ The South African study found proportional mortality ratio for lung cancer was raised in those miners with histological evidence of pulmonary fibrosis, but not otherwise.

While we find little to doubt as to the reliability of the scientific methodology represented in Plaintiffs’ Exhibit 18, of the three exhibits, Plaintiffs’ Exhibits 16, 17, and 18, it is the only one representative of the type of epidemiological study sufficiently reliable under the Havner/Robin-son standards. However, the Havner Court noted that it was not holding a single reliable epidemiological test is legally sufficient evidence of causation. Hav-ner, 953 S.W.2d at 718. “Careful exploration and explication of what is reliable scientific methodology in a given context is necessary.” Id. at 719. In the instant case, the testimony from the Baileys’ causation experts does not include any “careful exploration and explication” of what is reliable scientific methodology in the context of epidemiological studies linking asbestos exposure to a subsequent lung cancer diagnosis in a heavy smoker who is otherwise asymptomatic with regard to additional “typical” asbestos-related maladies.

More to the point, however, is the fact that neither of plaintiffs’ two causation experts made a sufficient showing that the relevant scientific community had generally accepted the theory of “synergism,” or even if accepted, that the scientific community had generally accepted the theory that there were no physical prerequisites to this “heavy smoking/asbestos exposure” synergism. Furthermore, what are we to make of the fact that each of the Baileys’ causation experts made James’s heavy smoking history at least equally responsible for his lung cancer as his asbestos exposure? Recall that Havner admonishes reviewing courts that, if other plausible causes exist that could be negated, plaintiffs must offer evidence excluding those other plausible causes of the injury or condition “with reasonably certainty.” Havner, 953 S.W.2d at 720.¹⁸ We are only left to conclude that there is no scientifically reliable evidence to support the verdict for the Baileys in this case. Mobil’s second issue is sustained. We reverse the judgment of the trial court and render judgment for Mobil.

REVERSED AND RENDERED.

1 . In March of 1998, the Texas Rules of Evidence, which govern both civil and criminal proceedings, replaced the former Texas Rules of Civil Evidence and Texas Rules of Criminal Evidence. As the current version of Rule 702 is identical to the pre-amendment version, all further references to Rule 702 will be to the current version.

2 . Rule 702. Testimony by Experts

If scientific, technical, or other specialized knowledge will assist the trier of fact to understand the evidence or to determine a fact in issue, a witness qualified as an expert by knowledge, skill, experience, training, or education may testify thereto in the form of an opinion or otherwise.

3 . See Cano v. Everest Minerals Corp., 362 F.Supp.2d 814, 821 (W.D.Tex.2005) ("However, Havner was not concerned with the admissibility of expert testimony, but the legal sufficiency of that evidence, although the inquiries are conflated under Texas law in the context of expert testimony.”) (emphasis in original).

4 . Eugene J. Mark, M.D. & Dong-Hwan Shin, M.D., Asbestos and the Histogenesis of Lung Carcinoma, 9 Seminars in Diagnostic Pathology, No. 2, 110-116 (May 1992).

5 . Id. at 110.

6 . Id. at 113.

7 . Id. at 114.

8 . Id.

9 .Jerrold L. Abraham, M.D., Commentary, Abestos Inhalation, Not Asbestosis, Causes Lung Cancer, 26 Am. J. Indus. Med. 839-42 (1994).

10 . Id. at 841.

11 . Id. (emphasis in original).

12 . Id. at 839.

¹³

14 . Paul Wilkinson et al., Is Lung Cancer Associated With Asbestos Exposure When There Are No Small Opacities on the Chest Radiograph?, 345 The Lancet 1074-78 (April 29, 1995).

15 . Id. at 1074.

16 . Id. at 1077.

¹⁷

18 . Assuming only for the sake of argument that a "synergistic effect” between James’s asbestos exposure and his heavy smoking was proven, this would not "negate” the undisputed role heavy smoking played in his development of lung cancer but would apparently accelerate the role his asbestos exposure played, if any, in his lung cancer.